dr Khaled selim lecture 2011

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dr Khaled selim lecture 2011

  1. 1. 110509 Khaled M. Selim In the Name of Allah,the Most Beneficent, the Most Merciful.
  2. 2. Curriculum Vitae (C.V.)Dr: Khaled Mohamed Selim Mohamed Abd Elrahman Lecturer of Fish Diseases and Management Faculty of Veterinary Medicine Zagazig University, EgyptAcademic Qualification :1- Bachelor of Veterinary Medical Sciences (B.V.Sc) May, 1998 from Zagazig University, Grade Very good.2- Master of Veterinary Medical Sciences (M.V.Sc), Fish diseases and management since, July 27, 2002 from Zagazig University.Title: Studies on Some factors affecting health and survival of Ornamental fish.3- Doctor philosophy of Science (Ph. D.), Reproductive biology of fish, March 23, 2009 from Niigata University, Japan.Title: Effects of temperature and methyl testosterone on sex reversal of fish.4- Post-doctoral researcher for a year (2009 –2010), in Department of Environmental Science, Fac. of Science, Niigata University, Japan.
  3. 3. Fish diseases
  4. 4. Parasitic DiseasesExternal or Internal orEctoparasitic EndoparasiticAffect head, fins, skin, eye, opercula, internal organ- blood – swimbuccal cavity, the surface of nasal bladder and deeper layer ofepithelium or olfactory epithelium, musclescrypts of the acoustolateralis systemor gills.
  5. 5. Metazoal Diseases Lerneosis Ergasilosis Argulosis
  6. 6. Endoparasitic MetazoaDigenetic trematode Cestode Nematode Parasitic cataract Ligulosis ContracaecumYellow grub disease Diphylobothriasis AmplicaecumBlack spot disease Anasakiasis Blood fluke Acanthocephala
  7. 7. 1-Monogenetic trematodes• Diseases of bad water quality• Affect external surface of fish• Affect freshwater and marine water by direct contact• direct life cycle• All are hermaphrodites• the attachment occurs by haptor ( Opisthaptor- Prohaptor)• They mainly fed on tissue debris and blood
  8. 8. Etiology and suscebitability Dactylogyrus spp (gill fluke) up to 2mm Gyrodactylus spp (Skin fluke) measure up to 0.4mm Benedenia and Neobenedenia spp mainly affect marine fish (oral and cutaneous fluke) 5-12 mm Dermophthrius spp mainly affect shark
  9. 9. •Theidentification ofmonogeneadepends on2. Haptorstructure
  10. 10. 2- Eye spotsor pigments3- Body size
  11. 11. 4- Alimentarytract structure5- Reproductiveorgan[oviparous orviviparous]6- Site andmode ofattachment
  12. 12. 7- Feeding behavior
  13. 13. very small eye spots8- Host specificity,geographical distributionand season Benedenia and Neobenedenia spp
  14. 14. Life cycle
  15. 15. Life cycle Dactylogyrus species at 24-28°C life cycle will be around 11-13 days Mature eggs developed within 2-3 days Post-oncho-miracidium is sexually matured in 4-5 days.
  16. 16. Epizootiology  Mechanical transmission by birds, reptile and amphibians  Nets and buckets are vehicle of transmission
  17. 17. Clinical signsI. General signs Affected fish appear lethargic abnormal swimming behaviors. Loss of reflexes Dark coloration especially in heavy infection Lower condition factor in long heavily infected fish
  18. 18. Abnormal swimming and movement
  19. 19.  Loss of appetite Remain at the side or bottom of the pond Restlessness Listlessness Emaciation Hyperirritability
  20. 20. II. General signs of body surface affections Irritation of skin Swim against water current Scratching body against any hard objects Copious quantities of mucous Loss of scales
  21. 21. • Minute abrasions or erosion Sometimes small ulcer hyperemia at the base of the fins Sometimes secondary invaded by bacteria or fungi
  22. 22. III. General signs of gill affections Aggregate on water inlet Aggregate on water surface Gasping of air Increase opercula movement
  23. 23.  Vertical swimming Jump outside water Die with open mouth Infected gills sometimes appear pale or be covered by whitish patches
  24. 24. Economic importance Affect all types of fish Mechanical damage due to hooks Mechanical carrier for bacterial and viral agent Secondary bacterial or fungal invasions Eye affections lead to blindness Decrease growth rate Individual Mortalities Aggregation of ration may lead to high ammonia level
  25. 25. Diagnosis• History• clinical sign and PM lesions• Parasitic examination• Molecular examination
  26. 26. A) Prevention Prophylactic measurements. predisposing cause source of infection.Quarantine and restriction of movement of fish -1. Good water quality -2.Reduction of over crowding of fish -3 .Proper nutrition of fish -4/ Periodical disinfection of ponds by 120 kg quick lime -5 .hectar .Control of aquatic plants -6.Control of organic matter -7All utensils such as nets, buckets, aereators, must be -8.disinfected .Regular examination of fish for parasites -9
  27. 27. B) Treatment and control Prophylactic spray of chemical agents starting at mid-April up to end of July as dipterex. Ammonia can reduce infection so can be used in ammonia tolerant fish as Japanese eel (40 ppm) Chemotherapy3. Dipterex: prepare 50% solution in xylene and apply it to the pond at a dilution of 0.8ppm.4. Potassium permanganate 20ppm with 4% Nacl5. Methylene blue, Malachite green formalin, Ammonium hydroxide, masotene….etc
  28. 28. Metazoal Diseases Ectoparasitic MetazoaMonogenetic Hirudinea Crustacean trematode or leech or Copepode Lerneosis Ergasilosis Argulosis
  29. 29. 2- Hirudinea – leech – Annelid Parasites of fish, worm amphibians and aquatic reptiles ( in both fresh and marine water) blood suckling parasites affect body surface, fins, gill or mouth cavity. Carried to the farm through contaminated water Bisexual temporary parasites
  30. 30.  Can be seen by naked eye (2-4 cm) and swim actively to reach the prey Body formed from several segments and has 2 suckers( anterior contains mouth and posterior contains suckers for attachment) They are temporary or semi permanent Leave after the meal Leave for cocoon searching for shelter deposition
  31. 31. Etiology / susceptibility Class: Hirudinea Phylum: Annelida Subphylum: Clitellata order: Rhynchobdellida (Most important) 1) Family: Piscicolidae (Cylendrical leech) – 4-8 cm 2) Family: Glossiphoniidae (flat leech)- 2-4 cm
  32. 32.  The identification of leeches depends on2. Body shape3. Length of the body4. Pigmentation colour and pattern5. Numbers and arrangement of the eyes
  33. 33. 5- Crescent form pigments on the body and caudal suckers.6- Arrangement of papillae or tubercles.It is better to examine the leech in fresh and relaxed state• We can use alcohol or menthols crystals for short time in a Petri dish before the change of pigment colors
  34. 34. Life cycle Male put sperms through spermatophore in female gonopore Mating occures on or off the host fish Fertilized egg will be attached to female body (within a special socket) or deposited on aquatic substrate (??) in the form of cocoons(1-5). Off springs can survive for a week or more before their first blood meal The period of nursing varies from 24 days – 4 months according to water temperature After nursing leech need 3- 4 blood meals to reach maturity
  35. 35. Clinical signs and Leech as it is can be seen pathology by naked eye Site of affection appears well defined rounded and sometimes oozed blood General sign of anemia especially in young fish ( thin body, emaciation, big head…) HB content drop from 50 to 20% RBCs count drop from 1.5 million to 300000/ml2.
  36. 36. Economic importance Affect all types of fish Young fishes are more seriously affected especially that live in the bottom….lead to reduction in vitality and death ( so it will lead to great damage to hatcheries). Mechanical damage to skin and scale pockets (sever epidermal erosions) due to suckers followed by Secondary bacterial or fungal invasions Vector transmitter for haemoprotozoa Mechanical transmission of viral and bacterial diseases Leech can suckle about 150 ml of blood within 2 days leading to marked anemia Produce Hirudin enzyme that acts as anticoagulant leading to oozing of blood from fish after leech leaving host A predisposing cause for opportunistic pathogen Decrease growth rate Individual Mortalities
  37. 37. Diagnosis• History• clinical sign and pathology• Parasitic examination• Molecular examination
  38. 38. Treatment and control Prophylactic: remove aquatic vegetations, apply net with small mesh size to prevent leech or gravels and stone entrance with water, summer drying season (chlorinated lime is able to destroy both live leech and cocoons), Chemotherapy3. Dipterex: prepare 50% solution in xylene and apply it to the pond at a dilution of 0.8 ppm.4. Masotene: 0.5-1 ppm in fish pond but harmful to zooplankton.5. Neguvon 1ppm for 5 days is effective against adult leeches but not eggs6. We can use OPC or chlorine* Marine water leeches have very little trials for treatment.
  39. 39. Metazoal Diseases Ectoparasitic MetazoaMonogenetic Hirudinea Crustacean trematode or leech or Copepode Lerneosis Ergasilosis Argulosis
  40. 40. III- Copepodes – Parasitic crustacea Many of crustacean parasite are lethal under certain circumstances, other depilating and other of major importance to fish culture and the fishing industry It showed exoskeleton with jointed appendages and segmented body. Affect mainly external surface of body. Many of parasitic copepods burrow into the flesh and cannot be dislodged by chemical treatment Treatment is directed toward killing larval forms.
  41. 41.  Oviparous parasites with separate sex They have a complex life cycle which involves mating of the parasites and attachment of the female to the fish with subsequent production of eggs which pass through several distinct larval stages. The most important organisms are:4. Lernea5. Ergasilus.6. Argulus
  42. 42. General life cycles of Crustacean parasites Mature male or female Fertilized eggCopepode stages napuli Meta napuli
  43. 43. 3- Lerneosis - Anchor worm Are the most harmful parasite of cultured fresh water fishes They most commonly found in warm water fish The destructive activity of lernea is due to its relatively large size and its mode of attachment and feeding
  44. 44. Etiology and suscebitability The are long slender copepod give the appearance of soft strikes with two eggs sacs attached at the end of the body the head is buried in the flesh by large horn-like appendages ]anchors} that help in identification of the parasite
  45. 45. • Affect mainly freshwater fish• There was two common species which include• Lernea cyprinacea (host specific) affect carp fish and accidentally other fish species• Lernea elegans (non host specific)
  46. 46. Life cycle• infective stage id 3rd copepode stage• Mature stage is 5th• mating occures on 6th copepode stage• male will die after mating while female will die afterproduction of 3 pairs of egg sacs or 20 days
  47. 47. The cycle will not be completed atthe following2.Temperature lower than 15ºC3.Drying4.Salinity of 1.8%5.Lower pH 7
  48. 48. Epizootiology Contaminated water, infected fish or carrier such as amphibians or birds.
  49. 49. Clinical signs and pathology be Lernea itself can seen by naked eyee They penetrate beneath scales and cause a lesion at the point of attachment (inflammation- hemorrhagic and erythematic lesion)
  50. 50. 3- Irritation- fish rub itsbody against hard objects- excessive mucous secretion4- General sign of fish diseases5. When affect gills lead to respiratory manifestation6. When affect eye lead to blindness7. When affect fins lead to difficult movement8. When large number of infestation occures within the same fish lead to emaciation and thinning
  51. 51. Economic importance Affect all types of freshwater fish Mechanical damage due to Anckors Secondary bacterial or fungal invasions Eye affections lead to blindness Decrease growth rate Individual Mortalities
  52. 52. Diagnosis History Clinical sign Parasitic identification Wet mount of skin or gills showing developing stages Molecular studies
  53. 53. 4- Ergasilosis- gill rot  crustacean parasite affect gill of fish.
  54. 54. Etiology and susceptibility Ergasilus spp most commonly found in warm water fish Affect freshwater and sometimes brackish water fish Carp fish less affected and increase in fish which live at the bottom Severity increase in high water temperature and lower salinity. Cyclopoid in shape Female only is parasitic
  55. 55. • Cant be easilyseen by naked eye.2mm• The antennae willbe transformed intohooks leading todamage of gilltissue……………..fedon blood and tissue
  56. 56. Life cycle• infective stage is 4th copepode stage• Mature stage is 5th• mating occures on 6th copepode stage• male will die after mating while female will dieafter production of 3 pairs of egg sacs or 20days
  57. 57. EpizootiologyHooks penetrate gill tissue leads to hyperplasiaInterfere in blood supply of the squamousepithelium and respiration in fishDifferent area of necrosis giving marblingappearanceEnded by sloughing of gill filaments
  58. 58. Clinical signs and pathology1.General sign of fish diseases2.Respiratory signs3.Marbling appearance of gill4.Parasite can be seen by wet mount preparation
  59. 59. Economic importance Highly significant epizootic of fish Mechanical gill damage due to hooks Secondary fungal and rarely bacterial invasions Decrease growth rate High Mortalities
  60. 60. Diagnosis History Clinical sign Parasitic identification under the microscope Molecular studies
  61. 61. 5- Argulosis- Fish lice- Branchiurans of fish Non specific Temporary parasites of skin, fins, gills or opercula mucosa It called fish lice due to it ability to creep about over the surface of fish Flattened against the side of the body Can be seen by naked eye Heavy infestation may lead to death even of large fish
  62. 62. Etiology and susceptibility Argulus spp affect both fresh and marine water fish Dorsal surface have a rigid or semi-rigid chitin exoskeleton Ventral surface has4. Two suction discs5. Four pairs of thoracic legs6. Two respiratory area7. No egg sacs
  63. 63. pre-oral sting which injects digestiveenzymes
  64. 64. Life cycle 7 molts to reach the adult
  65. 65. • After mating female leave hostand swim to aquatic plants or hardobjects to put egg with stickymucous material “sometimesmating occurs in water”.• life cycle take about 30-100 daysaccording to water temperature.• water temperature must beabove 16ºC for completion of lifecycle.
  66. 66. Epizootiology• Argulus feed by first inserting a pre-oral sting which injects digestive enzymes (or toxin produced from poisoning gland) into the body.• This toxin lead to tissue lysis, lymphocytic degeneration and break down of the skin.• They then suck out the liquidized body fluids with their proboscis-like mouth.
  67. 67. 4. This feeding activity causes intense irritation and localized inflammation5. Transmitted via water supply, mechanically by birds and amphibians
  68. 68. Clinical signs and pathology1.Fish lice are one of the biggest parasites (5-10 mm) and visible with the naked eye.2. The site of bite appears as red circular depression with raised margin ( Button like lesion)3. skin Hemorrhage and ulcer4. irritation and jump outside of water to get rid of parasite5. general sign of fish disease
  69. 69. Economic importance•They can cause significant morbidity andmortality• direct tissue damage• opportunistic bacteria such as Aeromonas orPseudomonas sometimes infect these damagedareas leading to skin ulcers and gill disease.• It is also believed that the stylus mayoccasionally ‘inject’ viruses and bacteria into thefish.• all these lead to severe stress, which oftenleads to secondary parasite infestations such aswhite-spot and Costia.
  70. 70. Diagnosis History Clinical sign Parasitic identification Histopathological section Molecular studies
  71. 71. A) Prevention of crustacean parasites1. Summer drying season The parasites will die if dehydrated. If a pond or tank is infected therefore, complete draining and leaving dry will kill off any parasites2. copper sulphate as prphylactive treatment3. Quarantine and restriction of movement of fish.4. Good water quality .5. Reduction of over crowding of fish.6. Proper nutrition of fish.7. Periodical disinfection of ponds by 120 kg quick lime / hectar.8. Control of aquatic plants.9. Control of organic matter.10. All utensils such as nets, buckets, aereators, must be disinfected.
  72. 72. Treatment and control1. Chemicals interrupt life cycle a chitin inhibitor drugs such as Dimilin will stop the juveniles developing as they moult their exoskeleton, most of the results have shown these compounds such as Lufenuron and Diflubenzuron to be entirely nontoxic to fish or other animals.2. The most common treatments are organophosphates, Masoten and Malathion. Using three treatments over the estimated life cycle of the parasite. At typical summer pond temperatures of 20ºC or higher, treatments at 10-day intervals will kill existing adults and juveniles as well as emerging juveniles.3. In small number reared fish mechanical removal of the parasites and dip in disinfectant (Potassium permanganate) and antibacterial drugs4. Potassium permanganate is useful in Ergasilus
  73. 73. Endoparasitic MetazoaDigenetic trematode Cestode Nematode Parasitic cataract Ligulosis ContracaecumYellow grub disease Diphylobothriasis AmplicaecumBlack spot disease Anasakiasiswhite grub disease Metacercarial disease Acanthocephala Blood fluke
  74. 74. 1- Digenetic trematod• Trematodes that have a complex life cycle need one or morehost• Most digenetic trematodes are not a serious threat to fishhealth; however, their presence often renders the fishundesirable by consumers.• There are 2 main groups•Fish act as intermediate host: fish contain metacercaria orencysted metacercaria until will be eaten by final host such as: a- Diplostomum spathaceum, parasitic cataract, eye fluke b- Clinostomum species, yellow grub disease c- Apophilus donicus, black spot disease•Fish act as a final host: fish contain adult parasite andproduce egg that leave fish to complete life cycle.
  75. 75. General life cycle of digenetic trematode Die within hours
  76. 76. a- parasitic cataract - eye fluke Etiology and Life cycleDiplostomum spathaceumFinal host is aquatic birdsSite in the final host intestineFirst IH is snail as Limnia snailsSecond IH is FishSite in fish eye tissue
  77. 77. Epizootiology•The usual route of transmission from snail tohost fish is through water and activepenetration of the cercria• Very rare the transmission is possible by fishfeeding on snails containing cercariae.• This parasite lodges itself in the eye of a fishand induces cataract formation (from itsmetabolic waste) this in turn increasespredation on intermediate fish, because thefish is less able to get away from predator dueto its new vision handicap.
  78. 78. Clinical signs and pathology• The fluke occursin the lens and fluidportion of the fish’seye.• A popeyed effectis sometimescreated fromaccumulation offluids in theeyeball.(Exophthalmia)
  79. 79. • In advancedcases, the eyebecomes opaquewhite and thefish becomespartially or totallyblind.
  80. 80. This is a photo of a fish eye encysted with Diplostomum Spathaceum
  81. 81. B- yellow grub disease Clinostomum marginatum Etiology and Life cycle• Final host is aquatic birds• Site in the final3. infected fish is eaten by a fish-eating bird4. the fish passes down into the stomach of the bird5.the cyst walls are digested by enzymes.6.The freed grubs migrate up the esophagus to thetrachea or the mouth cavity. Or drop with faeces7.the grubs attach themselves and become sexuallymature adults.8.the bird thrusts its beak into the water to feed, eggslaid by the adults are released into the water.
  82. 82. First IH is snail as HelisomaSecond IH is Fish (Cercaria burrow throughthe skin and encyst forming encysted •metacercaria). Metacercaria released fromtheir cysts are large and yellow in color ,reaching up to 5-6 mm in length and 2 mm inwidthSite in fish under the skin, gills andmuscles sometimes in body cavity andinternal organThe grubs can live for four years inindividual fish.
  83. 83. If the cyst is broken open, a yellowish or whitish parasite will be found
  84. 84. Clinical signs and pathology1- Yellowish vesicle can be seen inskin, muscles, gills and sometimesin internal organs2- when affect gills show respiratorymanifestation3- general sign of fish sickness4- in human Inadequate cookinglead to haulzun disease
  85. 85. c- black spot disease- Apophilus donicus Etiology and Life cycleFinal host is aquatic birdsSite in the final intestineFirst IH is snail as PlanorbellaSecond IH is FishSite in fish skin, tail base, fins,and musculature
  86. 86. Clinical signs and pathology1. Variable sized black spots (1 to 3 mm) in the skin, tail base, fins, and musculature.• The metacercariae of the black grub become encapsulated by host tissue• melanophores surround the outer layers• the dark color of the embedded grub causes affected fish to have a “peppered” appearance2- Until the black grubs become encapsulated in the host, the host loses lipids (fats) and their oxygen requirements increase.• Heavily infected cold water fish often enter the winter months in lipid depleted (low fat) state; consequently, these fish have few energy reserves to last over winter and that would affect their ability to survive.
  87. 87. Economic importance1. These parasites normally do not kill fish except in case of vital organ, but may reduce the growth rate if heavily infested.2. The presence of digenetic trematodes often renders the fish undesirable by consumers.3. It leads to sporadic mortalities4. Fish will be easily predated by enemy5. Proper cleaning and cooking will render the parasite harmless to man.
  88. 88. Diagnosis History Clinical sign Parasitic identification• identify the metacercaria• cyst can be released by enzymatic excystation using hatching solution or digestive solution• Complete the life cycle or developed in their natural host Histopathological section Molecular studies
  89. 89. D- Blood fluke Sanguinicoloiasis Etiology and Life cycleFinal host is fishSite in the final flukes of the vascularsystem of freshwater and marine fish.First IH is snail as Limniafound in cyprinid and salmonid fish inwhich it is a serious pathogen,especially in cultured carp.
  90. 90. Etiology and life cycleBlood flukes(Sanguinicola) liveas adults (ingroups /solitary)in the arterioles ofthe bloodvessels of themesenteries,hepatopancreas,pericardium,eye, gill, andcaudal kidney ofsalmonoides andother fish species.
  91. 91. • These tiny worms lay eggs thatbecome trapped in the capillarybeds of the gills and other organswhere they developed intomeracidia• The ciliate miracidia burst fromthe gill to be eaten by theoperculated snail, the onlyintermediat host.• Cercaria emerge from the snailand penetrate fish to complete thelife cycle.
  92. 92. After Cercaria penetrate the skin pass toblood and then to internal organs causeinflammation and decrease thephysiological and mechanical efficiency ofthese organs. In some cases, they kill thehost.
  93. 93. Clinical sign and pathology Acute form occurs when heavy numbers of the1. parasites present in brachial BVS (Occlusion, thrombosis, rupture and necrosis) leading to respiratory manifestation and massive mortalities. subacute form occures when heavy numbers of2. the parasites present in kidney Bvs (Glomerular occlusion- chronic nephritis) leading to general symptoms of ascites Chronic form occures when small numbers of the3. parasites scattered in the different body organs leading to emaciation and anemia.
  94. 94. Economic importance1- Massive mortalities whenaffect fish in acute form2- loss of fish flesh3- anemia and fish becomepredisposed for opportunisticpathogens3- Damaged kidney andspleen
  95. 95. Diagnosis History Clinical sign Parasitic identification Histopathological section Molecular studies
  96. 96. Prevention and control All control measurements to metacercaria are difficult because of the complexity of the life cycle, shortage of blood supply and disease condition. There is no known control of digenetic trematodes in ponds, other than the possible control of the snails and the birds
  97. 97. The following will help in the reduction of the occurrence.1- Control of snailsA- Mechanical control4.aquatic vegetation act as a food and shade for snails so the reduction ofaquatic vegetation will interrupt the life of snails.5.The water inlet should have a small mesh size to avoid introduction ofsnails to the pondB- Biological control7.Rearing of some snail eating fish such as snail carp8.Rearing of some duck and geese that fed on snails9.Some viruses and fungi that is fatal to snails and save to fish10.Snails that fed on snails but not act as IH for fish pathogeneC-Chemical control•Copper Sulfate used to control both snails and algae but should not harm fish•OPC and CHC2- Aquatic bird control• control the disease in the surrounding birds• Deep water at the pond edge discourages birds that feed in shallow water3- Summer drying season
  98. 98.  Monogenean infestations are more dangerous or digenean infestations2. Have a direct life cycle.3. Mode of attachment.4. Rapid multiplication.
  99. 99. Endoparasitic MetazoaDigenetic trematode Cestode Nematode Parasitic cataract Ligulosis ContracaecumYellow grub disease Diphylobothriasis AmplicaecumBlack spot disease Anasakiasiswhite grub disease Metacercarial disease Acanthocephala Blood fluke
  100. 100. Cestodes of fish Ribbon like parasite, divided into scolex, neck and stroblia Fish may be act as final host: present in the intestine and pyloric caeci of fish as sexually mature worm eg Proteocephalus Fish may be act as IH: larval form (plerocercoid ) present outside intestine4. vital organ ( Brain, heart ..)5. Less vital ( body cavity, visceral organs and muscle) it will be dangerous in large numbers
  101. 101. Life cycle
  102. 102. 1- Ligulosis Ligula intestinalis larvaFinal host is aquatic birdsSite in the final intestineFirst IH is copepodes as cyclopSecond IH fish body cavity (length 20-40 cm, width 0.5-1 cm and express 10% of body weight).Perch, pike perch, numerous cyprinids and trout are susceptible
  103. 103. Clinical sign and PMlesions1. Reduced growth and emaciation2. Anemia and dark coloration3. Enlargement of the abdomen in post cephalic region4. Peritonitis and atrophy of internal organ5. internal organs showed hemorrhage, necrotic white areas and ascites.
  104. 104. 2- Diphylobothriasis Diphylobothrium latum affect fresh water and marine water fishThis is the longest tapeworm found in man, ranging from 3-10 meters with more than 3000 proglottids.Final host are man sometimes fish eating mammals such as dog and catSite in the final intestine (3-10 m)First IH is copepodes as cyclop and diatoms (500 um)Second IH fish such as (pike, perch, salmon, trout and eel)
  105. 105. Hexacanthembryo
  106. 106. Etiology and Life cycle Eggs discharged from gravid proglottids in the small intestine of final host are passed in the feces. The egg hatches in fresh water to produce a ciliated coracidium which needs to be ingested by a water flea (Cyclops) where it develops into a procercoid larva. When infected Cyclops are ingested by the freshwater fish, the procercoid larva penetrates the intestinal wall and develops into a plerocercoid larva Man and other animals are infected by eating uncooked fish, mature into adult worms in 3 to 5 weeks.
  107. 107. Clinical signs1. Plerocercoids are found encysted or lying in the viscera and musculature of marine and fresh water fishes.2. migrating larvae can cause much damage with adhesions, sterility and even mortality3. The presence of this cestode affect the market value of fish.
  108. 108. Economic importance ofcestodes Migratory larval stages leads to peritoneal adhesions or damaged viscera because of pressure necrosis, other species may affect eye leading to blindness Poor growth and chronic mortalities Sterility and stop spawning Miserable appearance of fish affect marketing (Diphyllobothrium latum) can have hypochromic anaemia because it takes up vitamin B12, which is necessary for red blood cells to mature
  109. 109. Diagnosis History Sign PM lesions Parasitic identification Molecular study
  110. 110. Prevention and control Prevent human being from infection by Freezing for 24 hours, thorough cooking or pickling of fish kills the larvae. Fish reservoirs should be kept free of raw sewage Treatment of adult worms in final host using suitable anthelmentic drugs
  111. 111.  If fish act as final host, use:• Di-N-butyl tin oxide 0.5- 0.6 %of diet for 3 days• Praziquantel bath 2 mg / liter for 1 - 3 hoursor oral 50 mg / kg body weight / day Summer drying season for copepode control
  112. 112. Nematodes of fish It is cylendrical parasites with separate sex Either oviparous or viviparous Fish may be act as a final host or intermediate host or both at the same time The larval form in fish either uncapsulated or capsulated by host CT When fish act as final host the mature parasite will be found in the intestine When fish act as IH the parasite will be found in the abdominal cavity or musculature
  113. 113.  When fish act as IH it will be more dangerous than FH where it will usually affect a vital organ not intestine as well they infect the tissue and cause tissue damage during its migration Nematodes are more noticeable than other endoparasites due to their cuticle are more resistant to the post mortem autolytic enzyme in the dead fish and remain alive. The most common nematodes are4. Contracaecum5. Amplicaecum6. Anasakis
  114. 114. A- Contracaecum Mesentry worm disease• affect mainly freshwater fish, sometimesbrackish• Final host fish-eating birds, marine mammalsand sometimes carnivorous fish.• Site in the final intestine• First IH is copepodes as cyclop• Second IH fish• Site in fish in the body cavity and mesenteries• human act as a reservoir host if ate uncookedinfected fish
  115. 115. B- Amplicaecum Heart worm disease• affect mainly freshwater fish•Site in fish in the body cavity and mesenteriesmainly in the pericardium and heart
  116. 116. Clinical sign and PMlesions1. encapsulated larval form of variable size in tissues2. Round worms (red or white ) are found within the encapsulation and the lesions3. Free, non-encapsulated worms also occur in the abdominal and pericardial cavity and in sinus venosis (in case of heart worm disease)4. necrotic lesion in the dermis, the sub dermis and visceral organs5. deformed or atrophic gonads.
  117. 117. C- Anasakiasis Herring worm disease• occur worldwide and all species offish are susceptible.• common in marine mammalsespecially Herring fish.
  118. 118. The infected crustacean is subsequentlyeaten by a fish or squid, and the nematodeburrows into the wall of the gut and encystsin a protective coat, usually on the outside ofthe visceral organs, but occasionally in themuscle or beneath the skin.
  119. 119. Clinical signs and PMlesions1. In the live fish larvae may be free or coiled in capsule of host connective tissue2. Distension of abdomen will be observed OR sometimes affected fish show no external signs3. They can be found on or in the viscera, body cavity, skeletal muscles and mesenteries
  120. 120.  If third stage larvae consumed in row or inadequately cooked fish, it will cause2. serious gastrointestinal damage3. acute pain4. vomiting5. Diarrhea and blood in stools6. fever.7. Larvae can penetrate the digestive tract and enter the body cavity.
  121. 121. Economic importance1. decrease the commercial value of affected fish2. Cause many diseases in fish and man3. Larval migrations lead to dangerous effect on vital organ4. Poor growth and chronic mortalities5. Sterility and stop spawning
  122. 122. Prevention and control of Nematode1. Anisakiasis can be avoided by rapid evisceration and preparation fillets, deep freezing to -30 and sufficient marination or thorough cooking2. Regular examination of fish for parasites.3. Mature parasite use:• Fenbendazole orally 25 mg / kg body weight / day for 3 days or prolonged immersion 2 mg / liter• Levamisole HCL orally 2.5 – 10 mg (8mg) / kg body weight / day for 7 days or prolonged immersion 10 mg / liter
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